ABSTRACT
Autoimmune thyroid diseases [ATD] are multifactorial conditions that result from genetic predisposition in combination with environmental risk factors. Helicobacter pylori infection as an environmental risk factor has been proposed to imitate the antigenic components of the thyroid cell membrane and may play a leading role in the onset of the autoimmune diseases, such as Hashimoto thyroiditis. The aim of this study was to investigate the association between Helicobacter pylori [HP] infection and Hashimoto's thyroiditis [HT]. The participants in this case-control study included 43 patients affected by Hashimoto's thyroiditis, and 40 healthy individuals without history of autoimmune disease as the control group. Anti HP IgG and anti-TPO antibodies were determined using ELISA method. Results were considered positive when the IgG anti-HP value was higher than 30 lU/ml and the anti-TPO autoantibody value was higher than 75 lU/ml. The mean TSH level was 18.3 +/- 16.8 lU/ml for patients and 2.8 +/- 1.2 lU/ml for the control group [P<0.001]. 46.5% of the patient group and 10.8% of the control group were infected with HP. The association between HP and Hashimoto's thyroiditis was statistically significant [Odds Ratio=7.2, 95%, Confidence Interval: 2.0- 28.8, P<0.001]. The findings show that, there is an association between HP and Hashimoto's thyroiditis. To establish a definite correlation between them, more detailed studies with a more specialized examination and precise consideration regarding species of HP, genetic polymorphism of the host and investigation of environmental factors are needed
ABSTRACT
Diabetes mellitus is a global health problem affecting 366 million people worldwide and its prevalence is growing rapidly. Diabetic eye disease is present in up to 25% of diabetic subjects. Diabetic retinopathy is a chronic complication of diabetes that can result in blindness. Generally, there are two stages of diabetic retinopathy, non-proliferative and proliferative. The longer a person has diabetes and the poorer metabolic control, the higher the chance of developing diabetic retinopathy. The majority of people with type 2 diabetes will ultimately develop diabetic retinopathy. Multifactorial therapy targeted to lifestyle modification and optional glycemic control reduces the risk. However, diabetic retinopathy develops or progresses with time. Primary [preventive] strategies include glycemic, lipid, and blood pressure control. Glycemic control effectively reduces the incidence of diabetic retinopathy. In additional, its effect on progression of diabetic retinopathy has been demonstrated in randomized clinical trials. Furthermore, tight control of blood pressure significantly reduces the progression of retinopathy and visual loss. However, the Action to Control Cardiovascular Risk in Diabetes [ACCORD] Eye Study Group has shown that intensive blood pressure control has no beneficial effect on reducing the rate of diabetic retinopathy in subjects with type 2 diabetes. Elevated serum lipids and dyslipidemias are associated with a higher risk of diabetic retinopathy. The beneficial effects of lipid-lowering agents on the progression of retinopathy have been reported. Intensive combination therapy for dyslipidemia has been shown to effectively reduce the rate of progression of diabetic retinopathy in type 2 diabetes. Secondary strategies are focused on various pathophysiologic approaches such as blockade of the renin angiotensin system [RAS], anti-vascular endothelial growth factor agents, somatostatin analogues, protein kinase inhibitors, and anti-inflammatory agents. The purpose of the current overview is to look into the medical management of diabetic retinopathy, and to explore the primary [preventive] measures as well as secondary strategies proposed to be effective in its medical management